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GHRP-6

Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

A synthetic hexapeptide that stimulates growth hormone secretion by mimicking ghrelin and binding to GHS receptors in the pituitary gland.

Quick Stats
Studies 702
Trials 0
Formula C46H56N12O6
Overview Studies 702 Clinical Trials 0
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pubmed Jan 13, 2021

Ghrelin Affects Gastric Cancer Progression by Activating AMPK Signaling Pathway.

Hu. Xiao-Lin XL; Zhu. Yong-Jun YJ; Hu. Chang-Hua CH; You. Li L; Wu. Juan J; He. Xiao-Yan XY; Huang....

As the endogenous ligand for the GH secretagogue receptor (GHSR), Ghrelin is aberrant expressed in multiple malignant carcinoma, and involved in regulating a number of progression of cancer, especially in metastasis and proliferation. However, the precise role of Ghrelin in tumorigenesis of gastric cancer (GC) is still poorly understood. In this study, we extensively investigated the roles and mechanisms of Ghrelin in human gastric cancer. Ghrelin levels in cancer tissues and cell lines were analyzed by immunohistochemistry, qRT-PCR, and Western blot. Functional studies were performed after Ghrelin overexpressed or knockdown in AGS cell line. Cell proliferation was evaluated in by MTT and clone formation assays. The wound healing and Transwell system were used to assess the cell migration and invasive ability of GC cells. Cell apoptosis was detected by flow cytometry, and metabolic assays were performed to reveal the function of Warburg effect in the process. Ghrelin was lowly expressed in gastric cancer tissues and cell lines. Overexpression of Ghrelin inhibited gastric cancer cell proliferation, migration, invasion, and promoted apoptosis by activating the AMPK pathway, while D-[lys3]-GHRP-6 (a GHSR agonist) treatment relieved the effect, promoting tumorigenesis. Ghrelin knockdown increased the glucose uptake and lactic acid release, suggesting that Ghrelin elicited an anti-Warburg effect via AMPK pathway to inhibit gastric tumorigenesis. Ghrelin inhibits cell proliferation, migration, and invasion by eliciting an anti-Warburg effect via AMPK signaling pathway in gastric cancer cells.

pubmed Jun 8, 2023

Inhibition of ghrelin activity by the receptor antagonist [D-Lys3]-GHRP-6 enhances hepatic fatty acid oxidation and gluconeogenesis in a growing pig model.

Zhang. He H; Yan. Xiaoxi X; Lin. Ailian A; Xia. Pengke P; Su. Yong Y

Blocking the hunger hormone ghrelin with the antagonist [D-Lys3]-GHRP-6 in growing pigs lowered weight gain and made fat cells smaller. It also kicked up fat breakdown, liver fat burning, and glucose production, but it raised insulin and signs of insulin resistance. The results show how ghrelin influences metabolism, but they don’t give a clear, safe protocol for people to follow yet.

pubmed Sep 15, 2019

Ghrelin fiber projections from the hypothalamic arcuate nucleus into the dorsal vagal complex and the regulation of glycolipid metabolism.

Su. Manqing M; Yan. Meixing M; Gong. Yanling Y

This study aimed to explore the involvement of the ghrelin pathway from the arcuate nucleus (ARC) to the dorsal vagal complex (DVC) and to determine its role in the regulation of glycolipid metabolism. The protein and mRNA expression of ghrelin and growth hormone (GH) secretagogue receptor type 1a (GHSR-1a) were measured using immunohistochemistry and the polymerase chain reaction (PCR) method, respectively. Ghrelin fiber projections arising from the ARC and projecting into the DVC were investigated using retrograde tracing, combined with fluorescence immunohistochemical staining. The effects of electrical stimulation (ES) of the ARC on ghrelin-responsive, glucose-sensitive DVC neurons, glycolipid metabolism, and liver lipid enzymes were determined using electrical physiological method, biochemical analysis, quantitative real-time PCR (qRT-PCR) and Western blot analysis. GHSR-1a was expressed in the DVC neurons. Ghrelin fibers originating from the ARC projected into the DVC. ES of the ARC-activated the ghrelin-responsive glucose-excited (GE) and glucose-inhibited (GI) neurons in the DVC. ES of the ARC significantly elevated the serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and glucose levels; it reduced the serum high-density lipoprotein (HDLC) and insulin levels. Moreover, ES of the ARC increased liver acetyl-CoA carboxylase-1 (ACC-1) and decreased carnitine palmitoyltransferase-1 (CPT-1) expression, resulting in lipid accumulation in the liver. All the aforementioned effects were partially blocked by pretreatment with the ghrelin receptor antagonist [D-Lys-3]-GHRP-6 in the DVC and were reduced by vagotomy. ES of the ARC increased agouti-related protein (AgRP)/neuropeptide Y (NPY) expression in the ARC and ghrelin expression in the DVC. Ghrelin fiber projections arising from the ARC and projecting into the DVC play a role in the regulation of afferent glucose metabolism and glycolipid metabolism via the ghrelin receptor GHSR-1a in the DVC.

pubmed Oct 22, 2024

Ghrelin is involved in regulating the progression of Echinococcus Granulosus-infected liver lesions through suppression of immunoinflammation and fibrosis.

Zhu. Jiang J; Zhao. Hongqiong H; Aierken. Aili A; Zhou. Tanfang T; Menggen. Meng M; Gao. Huijing H;...

Cystic Echinococcosis (CE) is a zoonotic disease causing fibrosis and necrosis of diseased livers caused by infection with Echinococcus granulosus (E.g). There is evidence that E.g is susceptible to immune escape and tolerance when host expression of immunoinflammation and fibrosis is suppressed, accelerating the progression of CE. Ghrelin has the effect of suppressing immunoinflammation and fibrosis, and whether it is involved in regulating the progression of E.g-infected liver lesions is not clear. Serum and hepatic Ghrelin levels were observed in E.g-infected mice (4, 12 and 36 weeks) and compared with healthy control groups. Co-localization analysis is performed between protein expression of Ghrelin in and around the hepatic lesions of E.g-infected 12-week mice and protein expression of different hepatic histiocytes by mIHC. HepG2 cells and protoscoleces (PSCs) protein were co-cultured in vitro, as well as PSCs were alone in vitro, followed by exogenously administered of Ghrelin and its receptor blocker, [D-Lys3]-GHRP-6, to assess their regulatory effects on immunoinflammation, fibrosis and survival rate of PSCs. Serum Ghrelin levels were increased in E.g-infected 4- and 12-week mice, and reduced in 36-week mice. E.g-infected mice consistently recruited Ghrelin in and around the hepatic lesions, which was extremely strongly co-localized with the protein expression of hepatic stellate cells (HSCs), T cells and the TGF-β1/Smad3 pathway. The secretion of Ghrelin was increased with increasing concentrations of PSCs protein in HepG2 cells culture medium. Moreover, Ghrelin could significantly inhibit the secretion of IL-2, INF-γ and TNF-α, as well as the expression of Myd88/NF-κB and TGF-β1/Smad3 pathway protein, and promoted the secretion of IL-4 and IL-10. Blocking Ghrelin receptor could significantly inhibit PSCs growth in in vitro experiment. Ghrelin is highly expressed in the early stages of hepatic E.g infection and may be involved in regulating the progression of liver lesions by suppression immunoinflammation and fibrosis.

pubmed Jan 11, 2019

A Linear Fragment of Unacylated Ghrelin (UAG<sub>6-13</sub>) Protects Against Myocardial Ischemia/Reperfusion Injury in Mice in a Growth Hormone Secretagogue Receptor-Independent Manner.

Huynh. David N DN; Elimam. Hanan H; Bessi. Val&#xe9;rie L VL; M&#xe9;nard. Liliane L; Burelle. Yan Y...

Unacylated ghrelin (UAG), the most abundant form of ghrelin in circulation, has been shown to exert cardioprotective effect in experimental cardiopathies. The present study aimed to investigate the cardioprotective effect of a linear bioactive fragment of UAG against myocardial ischemia-induced injury and dysfunction in C57BL/6 wild type mice and the mechanisms involved. Treatments were administered at doses of 100 (UAG), 1,000 and 3,000 (UAG<sub>6-13</sub>) nmol/kg at 12 h interval during 14 days prior to 30 min left coronary artery ligation and reperfusion for a period of 6 or 48 h. The infarct area was decreased in a dose-dependent manner at 48 h of reperfusion, with a reduction of 54% at the highest dose of UAG<sub>6-13</sub> tested. Myocardial hemodynamics were improved as demonstrated by an increase in cardiac output, maximum first derivative of left ventricular pressure, and preload recruitable stroke work, a load-independent contractility index. Six hours after reperfusion, circulating levels of IL-6 and TNF-&#x3b1; pro-inflammatory cytokines were reduced, and the effect was maintained at 48 h for TNF-&#x3b1;. 5' AMP-activated protein kinase (AMPK) was activated, while acetyl-CoA carboxylase (ACC) activity was inhibited, along with a decrease in apoptotic protein levels. In isolated hearts, the effect of UAG<sub>6-13</sub> was unaffected by the presence of D-Lys<sup>3</sup>-GHRP-6, a ghrelin receptor (GHSR1a) antagonist, suggesting that the peptide acted through a GHSR1a-independent pathway. The results support the therapeutic application of UAG bioactive peptide fragments against myocardial ischemia/reperfusion injury.

pubmed Dec 7, 2022

The effects and mechanisms of ghrelin upon angiogenesis in human coronary artery endothelial cells under hypoxia.

Wang. Li L; Chen. Qingwei Q; Pang. Jun J

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor (GHSR), has been found to stimulate angiogenesis both in vivo and in vitro. However, the effect of ghrelin upon angiogenesis, and the corresponding mechanisms of ghrelin therein, in human coronary artery endothelial cells (HCAECs) under hypoxia is still unknown. Our study found that ghrelin significantly increased HCAECs proliferation, migration, in vitro angiogenesis, and microvessel sprouting from the aortic ring under hypoxic conditions. The ghrelin-induced angiogenic process was accompanied by vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2) and endothelial-specific receptor tyrosine kinase (Tie2) expressions. In addition, this angiogenic effect was almost completely inhibited by Ang-2 RNAi and Tie2 RNAi. Pretreatment with the GHSR1a blocker [D-Lys3]-GHRP-6 abolished ghrelin-induced VEGF, Ang-1, Ang-2 and Tie2 expressions and in vitro angiogenesis. In conclusion, this is the first demonstration that ghrelin stimulates HCAECs in vitro angiogenesis through GHSR1a-mediated VEGF, Ang-1, Ang-2 and Tie2 pathways under hypoxic conditions. It indicated that ghrelin might play an important role in myocardial angiogenesis after ischemic injury.